Creatinine clearance, the amount of protein in the urine, and serum amyloid A and C-reactive protein concentrations were determined regularly. Linear regression analysis showed a close correlation between the change in creatinine clearance each year and both serum amyloid A concentrations (20 patients: r= -083, p < 0001) and C-reactive protein concentrations (28 patients: r =-080, p< 0001). The correlation between serum amyloid A and C-reactive protein concentrations was also significant (317 parallel measurements: r-0-81, p < 0-001). These findings suggest that monitoring serum amyloid A or C-reactive protein concentrations is valuable in assessing the prognosis in secondary amyloidosis and that therapeutic measures that lower serum amyloid A concentrations may reduce the formation of amyloid.

ABSTRACT. A patient with seronegative rheumatoid arthritis developed a nephrotic syndrome. Histological examination of renal biopsy disclosed moderate amyloidosis. Ultrastructurally the glomerular amyloid deposits were seen to be located both within the mesangium and subepithelially in the peripheral capillaries. The patient was treated with prednisone and cyclophosphamide for two years. The nephrotic syndrome remitted and a follow‐up biopsy showed almost total disappearance of Congo red positive amyloid substance. Electron microscopy showed abundant finely granular material but only small amounts of fibrillar amyloid in the mesangial regions and intramembranous lucent areas containing few amyloid fibrils but no subepithelial deposits in the peripheral capillaries. We conclude that the mesangial amyloid substance was degraded to granular material and that the subepithelial amyloid deposits were resolved by mechanisms similar to those involved in the resolution of subepithelial immune complex deposits, i.e. through slow washing out and incorporation into the basement membrane.

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ABSTRACT. Two cases with different and not previously described fatal renal complications during treatment with penicillamine are reported. A man with seronegative rheumatoid arthritis with features of systemic lupus erythematosus was treated with penicillamine for six months and developed a mild membranous glomerulonephritis and a severe renal vasculitis leading to uremia and death. A woman with primary biliary cirrhosis was treated with penicillamine for nine months and developed a nephrotic syndrome, the renal biopsy showing minimal change glomerulonephritis. The nephrotic syndrome responded to prednisone but the patient died, probably from septicemia. Penicillamine may thus cause glomerular damage without deposition of immune complexes. A restricted use of the drug is recommended.

The clinical course of rheumatoid arthritis in the patient described was characterized by two episodes of microhaematuria, both occurring shortly after the administration of gold salt. The second of these episodes developed into progressive renal failure. Renal biopsy disclosed a rarely described granulomatous glomerulonephritis. Various known pathogenic mechanisms of renal injury are evaluated concerning their applicability in this patient. However, although it is believed that the gold salt therapy was the main agent in the pathogenesis of this fatal renal complication, the mechanism whereby such a pathogenesis proceeded remains unclear.